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Retrospective cohort study evaluates senescence burden in acute myeloid leukemia, suggesting implications for treatment strategies.
BACKGROUND: Chemotherapy constitutes the backbone of Acute Myeloid Leukemia (AML) treatment but often induces cellular senescence. While senescence initially halts tumor proliferation, the accumulation of senescent cells and the Senescence-Associated Secretory Phenotype (SASP) may promote leukemic survival and relapse. The clinical correlation between post-treatment senescence burden and AML prognosis remains poorly characterized. METHODS: expression, alongside Senescence-Associated β-galactosidase (SA-β-gal) activity using flow cytometry. Immune sub-clustering was performed to evaluate senescence in progenitor versus mature populations. SASP factors (IL-6, IL-8, TNF-α) were measured in bone marrow plasma by ELISA. Patients were stratified into High-Senescence and Low-Senescence groups based on median cut-off values. RESULTS: (HR 1.98, 95% CI 1.15-3.40) as independent predictors of poor prognosis. CONCLUSION: Therapy-induced senescence creates a pro-tumoral microenvironment via SASP in AML. High senescence burden post-induction is a robust biomarker for poor outcomes, suggesting that senolytic strategies targeting these cells could improve therapeutic efficacy.
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Ma et al. (2026) studied this question.
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